Saturday, February 28

What is madarosis?

Madarosis is the medical term for loss of eyelashes or loss of eyebrows.

Madarosis is a clinical sign caused by several disorders including, malnutrition, infections, genetic factors, autoimmunity and systemic diseases. The term madarosis includes both temporary loss of eyelashes or eyebrows and also permanent destruction of hair follicles. Depending upon the causative factor, madarosis can be scarring (permanent) or non-scarring.

Identification of the predisposing disorder may help in taking action to reverse madarosis. In scarring loss, the hair follicles are permanently damaged and are not capable of regeneration. Close observation in such madarosis will reveal, tissue damage, inflammation, atrophy and loss of follicular openings. Such situations require surgical management. Eyebrow grafts and follicular unit transplantation are some of the effective surgical procedures for eyelash loss.

The non-scarring type of eyebrow or eyelash loss, can be reversed with proper diagnosis and treatment. It is important to note that the hair of eyelashes and eyebrows go through the growth phases similar to scalp and other body hair.

The eyelash and eyebrow hair (cilia) is normally known to grow at the approximate rate of 0.15 mm per day and falls off in about six months. A new eyebrow hair may take about two months to grow after plucking.

Causes of madarosis

The loss of eyebrows or eyelashes may occur due to several causes, including malnutrition, infections, trauma, medications, cancer treatment, ophthalmic conditions and systemic conditions. Some of these madrosis causing factors are briefly discussed here.

Malnutritional madarosis

Chronic protein deficiency is associated with madarosis and telogen effluvium. Zinc is vital for hair health and its deficiency is known to cause general hair loss and madarosis in particular. Acrodermatitis enteropathica, a genetic autosomal recessive disorder, affects the ability of intestines to absorb zinc. It is characterized by dermatitis of natural orifices and limbs. Apart from gastrointestinal problems, this disorder causes loss of hair from scalp, eyebrows and eyelashes. Biotin and iron deficiencies show symptoms like loss of eyebrows and eyelashes.

Madrosis in infections

Loss of hair including eyelashes and eyebrows is the characteristic of lepromatous leprosy. Madarosis occurs in lepromatous leprosy due to histiocytic infiltration of hair follicles. Unilateral madarosis may occur in tuberculoid leprosy in the eyebrow/eyelash region due to granulomatous infiltration of hair follicles leading to their destruction and loss. Bacterial infections like secondary and tertiary syphilis can cause madarosis and hair loss.

Viral infections like herpes zoster and HIV/AIDS are known to cause alopecia of eyelashes and eyebrows. Paracoccidioidomycosis (also known as "Brazilian blastomycosis) is a fungal infection caused by the fungus Paracoccidioides brasiliensis and is associated with madrosis. Periocular tinea is another fungal infection involving eyes and is known to cause loss of eyelashes. Tinea capitis is a fungal infection of scalp and it can cause eyebrow loss.

Parasites and madarosis

Demodex folliculorum and Demodex brevis are species of face mites existing as commensals inside hair follicles and sebaceous glands. During a severe infestation, they may cause inflammation, facial hair loss and madarosis. Phthiriasis palpebrarum is an infection of the eyelids caused by the pubic louse (Phthirus pubis) leading to madarosis. Heavy infestation may cause loss of eyebrows and eyelashes.

Radiotherapy and madarosis

Radiotherapy for malignant tumors often causes hair loss, including eyelashes and eyebrows. The anagen phase of hair growth is disturbed by the radiation. In most cases the madarosis is reversible.

Chemotherapy

Chemotherapy for malignant tumors often causes hair loss, including eyelashes and eyebrows. The anagen phase gets abruptly gets terminated and without telogen resting phase the hair strand weakens and breaks. After completing chemotherapy, the madarosis condition ends and new hair start growing.

Ophthalmic conditions and madarosis

Ophthalmic diseases, inflammations and trauma can causes madarosis.

Blepharitis and loss of eyelashes

Blepharitis is a common eyelid inflammation, caused by seborrhoea, bacterial infection (staphylococcus) or meibomian gland dysfunction (MGD). The patient may suffer from itching, burning, photophobia and the sensation of the presence of foreign in the eyes. Madarosis may occur due to rubbing of the eyelids, eyelid margin inflammation or folliculitis. Entropion and ectropion of eyelids, stye (chalazion and hordeolum) ocular rosacea, conjunctivitis and cicatricial lagophthalmos can cause eyelid margin inflammation and madarosis.

Madarosis in dermatological conditions

Atopic dermatitis as well as seborrhoeic dermatitis can cause madarosis. In the eyelids, the condition may manifest as lid margin inflammation leading to eyelash loss. Alopecia of the eyebrows occurs due to erythema, pruritus and scaling leading to rubbing and scratching. Other dermatological conditions such as, psoriasis, lamellar ichthyosis, postmenopausal frontal fibrosing alopecia, primary cicatricial alopecias, lichen planopilaris, ulerythema ophryogenes, telogen effluvium, follicular mucinosis and cutaneous sarcoidosis can cause loss of eyelashes and/or loss of eyebrows.

Endocrine disorders and madarosis

Both hypothyroidism as well as hyperthyroidism cause madarosis. Thyroid malfunction is one of the well known cause of eyebrow loss and eyelash loss. Nina van Beek et al, in their study published in 'The Journal of Clinical Endocrinology & Metabolism. 2008 Nov;93(11):4381-8.', concluded that "we present the first evidence that human hair follicles are direct targets of thyroid hormones and demonstrate that T3 and/or T4 modulate multiple hair biology parameters, ranging from hair follicle cycling to pigmentation."

The 'Sign of Hertoghe' (aka Queen Anne's sign) is a thinning or loss of the outer third of the eyebrows which is considered as a sign of hypothyroidism. The thinning, breaking, shortening and loss of hair is one of the signs of hyperthyroidism. Other endocrine disorders like hypopituitarism, hypoparathyroidism and hyperparathyroidism may also cause loss of eyebrows and loss of eyelashes.

Systemic disorders and madarosis

Alopecia areata is a hair-specific autoimmune disease causing patchy loss of hair in the body and madarosis of eyelashes and eyebrows. In alopecia universalis, the eyebrows and eyelashes may be totally lost. Cutaneous lupus erythematosus, an autoimmune disorder, giving rise to scaly lesions and plaques may involve eyebrows, causing madarosis. Frontal linear scleroderma (also known as en coup de sabre) is a linear scleroderma characterized by a linear atrophy and a furrow in the facial skin causing loss of facial symmetry.

Eyebrow and eyelash loss has been reported in frontal linear scleroderma. Graham Little syndrome, possibly an immune disorder, is a rare variant of lichen planopilaris, an inflammatory form of scarring hair loss and madarosis. Familial acanthosis nigricans has been reported to cause alopecia. Parry–Romberg syndrome (also known as progressive hemifacial atrophy) is a rare neurocutaneous syndrome. An autoimmune mechanism is suspected to be the cause. It can cause madarosis. Vogt–Koyanagi–Harada syndrome is an multisystem autoimmune disease which may involve uveitis, poliosis and madarosis.

Psychiatric causes of madarosis

Trichotillomania is an impulse-controlled psychiatric disorder characterized by compulsive plucking or breakage of hair. Affected patients tend to pluck scap hair, pubic hair and eyebrows. They develop patches of alopecia and madarosis. Trichoteiromania yet another type of artificial hair loss, which results from perpetual rubbing of the scalp and othery parts. It may also cause madarosis.

Madarosis management

Management of loss of eyelash and eyebrows primarily depends upon treating the causative factor. In conditions where the hair does not grow back and also in scarring madarosis hair transplants and wearing false makeup are the alternatives for cosmetic purposes. In non-scarring madarosis, treatment with topical minoxidil or latanoprost may be tried under medical professional's guidance. Surgical management of the hair loss and madarosis by follicular unit transplantation and eyelash/eyebrow grafting
are being successfully carried out.

Wednesday, February 25

Do thyroid disorders cause hair loss?

Yes! Thyroid malfunction is one of the causes for hair loss.

The thyroid is an endocrine gland secreting the hormones, thyroxine (T4) and triiodothyronine (T3) into the bloodstream. Iodine is necessary for the production of thyroxine and triiodothyronine. The thyroid-stimulating hormone (TSH) produced by the pituitary gland stimulates the thyroid gland to produce T3 and T4.

Thyroxine (T4) is the main hormone produced by the thyroid gland; but it is less potent than T3. The thyronines act on nearly every cell in the body, including the hair follicles (HFs). Within the cells, much of T4 is converted into T3 by deiodinase (iodide peroxidase) enzyme, which is also involved in the activation or deactivation of thyroid hormones. Deiodinase and its isoforms are selenium-containing enzymes and selenium deficiency can impact T3 production.

Both insufficient and excess production of the thyronine hormones, can affect, alter or cause loss of the cell structure and function. This includes hair follicles and loss of their function. Nina van Beek et al, in their study published in 'The Journal of Clinical Endocrinology & Metabolism. 2008 Nov;93(11):4381-8.', concluded that "we present the first evidence that human HFs are direct targets of thyroid hormones and demonstrate that T3 and/or T4 modulate multiple hair biology parameters, ranging from HF cycling to pigmentation."

Hypothyroidism hair loss

Hypothyroidism is a common endocrine disorder in which sufficient thyroxine hormones are not produced. The common symptoms include, slow pulse rate, dry skin, hair loss, cool extremities, weight gain with poor appetite, abnormal sensation, irregular menstrual cycles, delayed puberty and poor hearing. Iodine deficiency is the most common cause of low thyroxine hormones.

Another common cause is Hashimoto's thyroiditis or chronic lymphocytic thyroiditis. It is an autoimmune disease in which the endocrine cells are attacked by the patient's immune bodies. The treatment is by hormonal replacement with agents such as levothyroxine or triiodothyronine. In some cases, women, post pregnancy get affected by postpartum thyroiditis causing low thyroid hormone levels.

Hyperthyroidism hair loss

An excess of circulating free thyroxine can cause a number of disorders. The pace of all the cellular processes in the body is speeded up. Some of the symptoms are nervousness, irritability, sweating, palpitation, hand tremors, anxiety, loss of sleep, thinning of the skin, fine brittle hair, loss of the outer third of the eyebrows, scalp hair breakage and loss, increased appetite, weight loss, digestive system hypermotility and muscular weakness.

Graves' disease (or Flajani-Basedow-Graves disease) is the major cause of excessive thyroxine production. It is an autoimmune disease affecting the thyroid glands causing their enlargement. Apart from affecting many organs, it causes bone loss by an increased excretion of calcium and phosphorus in the urine and stool. Graves' disease may cause ophthalmopathy with ocular manifestations such as soft tissue inflammation, proptosis and optic nerve compression. The optic nerve involvement may cause loss of vision.

The second most common cause of excess thyroxine production, after Graves' disease, is toxic multinodular goiter. There is excess production of thyroxine hormones from functionally autonomous thyroid nodules which do not require stimulation from TSH. Another cause of excess thyroxine production is toxic thyroid adenoma, a benign tumor of the thyroid gland.

Iodine is necessary for the body's growth and development. Iodine dietary insufficiency can affect several biochemical functions of the body including thyroid hormone production. Iodine deficiency can affect the proper functioning of several organs, including skin and hair follicles.

Iodine is important for the functioning of the thyroid glands. Thyroid hormones contain iodine and its deficiency can lead to insufficient hormone production and hypothyroidism (goiter). Hypothyroidism can lead to slow down in heart rate, dry skin, hair loss, dry hair, weakness, fatigue, depression, loss of memory and mental retardation. The extreme manifestation of the deficiency of the mineral is steep decline and loss in IQ and cretinism.

Marine products, including fish, kelp, seaweeds and shellfish are rich natural food sources. However people living far away from the coast tend to take low amounts of seafoods and develop insufficiency of the mineral in their system.

The insufficiency of this trace mineral is taken care of in several countries by compulsory iodization of the common table salt. The amount added to common salt is just to stave off hypothyroidism. Apart from thyroid glands, iodine is present in high concentrations in breast tissue, stomach lining cells, ovaries, prostate glands and oral mucosa. Any insufficiency will adversely affect the health of these tissues.

There is loss of considerable amounts of the mineral in storage due to heat and moisture. The increasing use of toxic halides like bromides, chlorides, perchlorate and fluorides reduces the natural availability of iodine as well as its utilization in the body.

Several studies on animals have demonstrated that the deficiency of the mineral can lead to poor growth of coat as well as hair loss. Potter BJ et al had reported that, "samples of wool removed from selected areas of the sheep showed that the iodine-deficient diet also caused a reduction in the growth of wool." Sheep grazing on lands poor in this mineral found to suffer loss in hair growth.

According to World Health Organization, "Iodine deficiency is the world’s most prevalent, yet easily preventable, cause of brain damage". "Iodine deficiency disorders (IDD), which can start before birth, jeopardize children’s mental health and often their very survival." World Health Organization has also related its deficiency to adverse consequences for human infertility.

The US Food and Nutrition Board of the Institute of Medicine recommended dietary allowance (RDA) for iodine is 150-290 micrograms (mcg) for adults and the tolerable upper limit is 1,100 mcg. Too much of the mineral can lead to hyperthyroidism causing several adverse effects.

Monday, February 16

Home › Telogen effluvium definition › Telogen effluvium regrowth - Telogen effluvium recovery.
Telogen effluvium (TE) type of hair loss in most cases is temporary and need no special treatment. The typical sign of telogen shedding is the presence of barely perceptible follicular bulb at the end of most of the shed hair strands.

There is diffuse shedding all over the scalp. Telogen effluvium is self-correcting and complete recovery and regrowth is possible. However the time taken for the recovery and regrowth varies widely among individuals. The telogen effluvium can be acute or chronic.

Acute telogen effluvium

Normally an individual loses between 50 to 100 strands in a day. Acute telogen effluvium may begins relatively abruptly with drastic increase in shedding. The increased shedding may start two to three months after the initiating episode. In worst cases even up to 70% of the strands may be lost. However there is no risk of balding. The typical decrease in shedding and the recovery and and regrowth may commence by about six months. There is a 95% chance of complete recovery from the acute telogen hair loss. Identifying the triggers and taking corrective measures may speed up recovery and regrowth as well as reduce the risk of recurrence.

Chronic telogen effluvium

For patients with chronic telogen hair loss, it is very difficult to predict the time frame for recovery and regrowth. The mental stress created by the chronic condition adds to the hair loss problem. Patients with chronic loss require a lot of reassurance. It is very difficult to see the light at the end of the tunnel as the recovery and regrowth in chronic cases are very gradual processes, may sometimes take years. Whatever form of telogen loss occurs, it is fully reversible and complete regrowth is possible.

Managing telogen effluvium

Analyzing the causative factors and triggers can help us in the better management of TE loss and also help in recovery and regrowth.

Use of contraceptives, certain antibiotics, anti-androgen medications, anticoagulants, antidepressants and anticonvulsants are known to cause telogen hair loss. The withdrawal of the inducing factors helps recovery and regrowth. In individuals with genetic predisposition for androgenetic alopecia, a bout of TE may induce or trigger androgenetic alopecia. In nutritional deficiency caused shedding, recovery and regrowth can be induced by supplementing the deficient nutrient.

Leading a relaxed life, sleeping well, taking balanced food and exercising regularly can reduce telogen hair loss and speed up recovery and regrowth.

Biotin deficiency

It was considered that biotin deficiency is fairly rare. However recent research has established that marginal insufficiency of vitamin B7 is much more common than it was thought in the past. The intestinal flora also synthesizes this vitamin.

Dietary insufficiency, loss of intestinal flora and decreased uptake from the intestines are the main causes of biotin deficiency.

Patients who have undergone surgical removal of part of intestine or stomach are prone to develop vitamin B7 insufficiency.

Severely malnourished children develop biotin deficiency.

Genetic mutations can cause decreased activity of certain proteins involved in absorption in intestines and reabsorption in the kidneys leading vitamin B7 insufficiency in the body.

Janos Zempleni et al reported that decreased activity of certain proteins such as "monocarboxylate transporter 1, sodium-dependent multivitamin transporter, the biotin protein ligase holocarboxylase synthetase and the biotin peptidyl hydrolase biotinidase" can precipitate biotin deficiency. These proteins play crucial role in the intestinal absorption of biotin, its transport in plasma, its renal reabsorption and in the regulation of histone biotinylation. Biotinidase is present in pancreatic fluids and intestinal secretions plays a critical role in releasing free biotin from biocytin and biotinylated peptides prior to absorption.

Biotin deficiency and hair loss

The consequences of vitamin B7 insufficiency occur slowly and cumulatively. Biotin is essential for maintaining a healthy skin and the skin appendages like hair, nails, sebaceous glands and sweat glands. Vitamin B7 deficient cells undergo senescence earlier than the normal cells. As the consequence, the hair growth is slowed down, with increase in daily loss of telogen strands.

Mitochondria has an important function in cellular senescence and aging. Vitamin B7 insufficiency causes loss of mitochondrial complex IV, which is the the main oxygen-metabolizing enzyme converting most of cellular oxygen to water. In biotin deficiency, the levels of oxidants and the oxidative damage increase leading to DNA damage and cellular senescence. Thus all the cells in hair follicles undergo cellular damage causing their loss in the event of biotin deficiency.